Dapagliflozin did not significantly reduce 6-month changes in remote myocardium extracellular volume fraction compared to placebo in STEMI patients (difference -1.82; 95% CI -4.86 to 1.23; P=0.235).
RCT (n=52)
Double-blind
Does dapagliflozin reduce myocardial fibrosis (measured by CMR-derived ECV) in patients with STEMI undergoing pPCI with LVEF ≤ 50%?
In patients with STEMI and LVEF ≤ 50% undergoing pPCI, dapagliflozin did not significantly reduce myocardial extracellular volume or fibrosis biomarkers at 6 months, though it may improve left ventricular end-systolic volume.
Effect estimate: Difference -1.82 (95% CI -4.86 to 1.23)
Absolute Event Rate: -0.39% vs 1.43%
p-value: p=0.235
Background: Myocardial fibrosis plays a key role in adverse remodeling after ST-segment-elevated myocardial infarction (STEMI). The effect of sodium–glucose cotransporter 2 inhibitors (SGLT2is) on myocardial fibrosis deposition among patients with STEMI undergoing primary percutaneous coronary intervention (pPCI) is unclear. Objectives: To assess the effects of SGLT2is on myocardial fibrosis among patients with STEMI undergoing pPCI. Methods: Patients with STEMI undergoing pPCI with left ventricular ejection fraction ≤ 50% were randomized to dapagliflozin 10 mg or placebo. The primary endpoint was cardiac magnetic resonance (CMR)-derived 6-month changes in remote myocardium extracellular volume (ECV) fraction from baseline. Secondary endpoints included changes in CMR-derived myocardial volumes, change in serum fibrosis biomarker levels, and adverse events. Multivariable adjustment for infarction location and diabetes status was performed as sensitivity. The study was halted prematurely due to slow recruitment. Results: Fifty-two patients underwent randomization between May 2021 and April 2024 and completed follow-up. At 6 months, dapagliflozin resulted in a non-significant reduction in ECV change compared to placebo (−0.39 4.7 vs. 1.43 5.7; difference: −1.82 −4.86; 1.23; p-value = 0.235) while also leding to a higher degree of reduction in N-terminal pro-peptide of type III collagen (−177.0 pg/mL 416.1 vs. 3.6 pg/mL 553.8; p-value = 0.208). No significant differences in other biomarkers or adverse events were noted in the main analysis. After adjustment, dapagliflozin was associated with increased reduction in left ventricular end-systolic volume (−4.02 mL 7.4 vs. 0.10 mL 10.1; difference: −4.92 −9.8; −0.1; p-value = 0.047). Conclusions: In STEMI patients undergoing pPCI, dapagliflozin did not result in a significant reduction in ECV or biomarkers of fibrosis at 6 months.
Ortega-Paz et al. (Sun,) conducted a rct in ST-segment-elevated myocardial infarction (STEMI) (n=52). Dapagliflozin vs. Placebo was evaluated on CMR-derived 6-month changes in remote myocardium extracellular volume (ECV) fraction from baseline (Difference -1.82, 95% CI -4.86 to 1.23, p=0.235). Dapagliflozin did not significantly reduce 6-month changes in remote myocardium extracellular volume fraction compared to placebo in STEMI patients (difference -1.82; 95% CI -4.86 to 1.23; P=0.235).